Linked Life Data

17261927

Source:http://linkedlifedata.com/resource/pubmed/id/17261927

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-2-16
pubmed:abstractText
In end-stage renal disease (ESRD) there is not only excessive morbidity and mortality due to cardiovascular disease but also an enhanced occurrence of various types of cancer. Both are characterized by oxidative stress and inflammation as two of the central underlying causes of the disease states. In cancer, genomic damage has been demonstrated to be of high pathogenetic relevance. DNA lesions may induce mutations of oncogenes and tumor-suppressor genes which, in the long-run, may lead to malignancies if mutagenicity is not mitigated by repair mechanisms. A high incidence of genomic damage in ESRD patients has been validated by various biomarkers of DNA lesions. We reviewed the mechanisms of DNA damage, focusing in particular on the role of advanced glycation end products (AGEs) which accumulate markedly in renal insufficiency. Considering the in vitro and in vivo findings to date, one has to assume a significant role of AGEs in DNA damage and the potential development of cancer.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1420-4096
pubmed:author
pubmed:copyrightInfo
Copyright 2007 S. Karger AG, Basel.
pubmed:issnType
Print
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
56-66
pubmed:dateRevised
2007-11-7
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Genomic damage and malignancy in end-stage renal failure: do advanced glycation end products contribute?
pubmed:affiliation
Department of Experimental and Clinical Pharmacotherapy, Research Base of Slovak Medical University, Bratislava, Slovakia. katarina.sebekova@szu.sk
pubmed:publicationType
Journal Article, Review